PMID- 19995898
OWN - NLM
STAT- MEDLINE
DCOM- 20100303
LR  - 20211020
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 78
IP  - 2
DP  - 2010 Feb
TI  - Genetic control of the innate immune response to Borrelia hermsii influences the 
      course of relapsing fever in inbred strains of mice.
PG  - 586-94
LID - 10.1128/IAI.01216-09 [doi]
AB  - Host susceptibility to infection is controlled in large measure by the genetic 
      makeup of the host. Spirochetes of the genus Borrelia include nearly 40 species 
      of vector-borne spirochetes that are capable of infecting a wide range of 
      mammalian hosts, causing Lyme disease and relapsing fever. Relapsing fever is 
      associated with high-level bacteremia, as well as hematologic manifestations, 
      such as thrombocytopenia (i.e., low platelet numbers) and anemia. To facilitate 
      studies of genetic control of susceptibility to Borrelia hermsii infection, we 
      performed a systematic analysis of the course of infection using immunocompetent 
      and immunocompromised inbred strains of mice. Our analysis revealed that 
      sensitivity to B. hermsii infections is genetically controlled. In addition, 
      whereas the role of adaptive immunity to relapsing fever-causing spirochetes is 
      well documented, we found that innate immunity contributes significantly to the 
      reduction of bacterial burden. Similar to human infection, the progression of the 
      disease in mice was associated with thrombocytopenia and anemia. Histological and 
      fluorescence in situ hybridization (FISH) analysis of infected tissues indicated 
      that red blood cells (RBCs) were removed by tissue-resident macrophages, a 
      process that could lead to anemia. Spirochetes in the spleen and liver were often 
      visualized associated with RBCs, lending support to the hypothesis that direct 
      interaction of B. hermsii spirochetes with RBCs leads to clearance of bacteria 
      from the bloodstream by tissue phagocytes.
FAU - Benoit, Vivian M
AU  - Benoit VM
AD  - Department of Molecular Genetics and Microbiology, University of Massachusetts 
      Medical School, Worcester, MA 01655, USA.
FAU - Petrich, Annett
AU  - Petrich A
FAU - Alugupalli, Kishore R
AU  - Alugupalli KR
FAU - Marty-Roix, Robin
AU  - Marty-Roix R
FAU - Moter, Annette
AU  - Moter A
FAU - Leong, John M
AU  - Leong JM
FAU - Boyartchuk, Victor L
AU  - Boyartchuk VL
LA  - eng
GR  - R21 AI037601/AI/NIAID NIH HHS/United States
GR  - R01 AI037601/AI/NIAID NIH HHS/United States
GR  - AI37601/AI/NIAID NIH HHS/United States
GR  - AI060991/AI/NIAID NIH HHS/United States
GR  - R01 AI060991/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20091207
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
SB  - IM
MH  - Anemia/genetics/microbiology
MH  - Animals
MH  - Disease Progression
MH  - Female
MH  - Flow Cytometry
MH  - *Genetic Predisposition to Disease
MH  - Immunity, Innate/*genetics
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Relapsing Fever/*genetics/*immunology/pathology
MH  - Sex Factors
MH  - Thrombocytopenia/genetics/microbiology
PMC - PMC2812184
EDAT- 2009/12/10 06:00
MHDA- 2010/03/04 06:00
PMCR- 2010/08/01
CRDT- 2009/12/10 06:00
PHST- 2009/12/10 06:00 [entrez]
PHST- 2009/12/10 06:00 [pubmed]
PHST- 2010/03/04 06:00 [medline]
PHST- 2010/08/01 00:00 [pmc-release]
AID - IAI.01216-09 [pii]
AID - 1216-09 [pii]
AID - 10.1128/IAI.01216-09 [doi]
PST - ppublish
SO  - Infect Immun. 2010 Feb;78(2):586-94. doi: 10.1128/IAI.01216-09. Epub 2009 Dec 7.